In this study, the mechanism of $H_2S$ protection in the hippocampus of heroin-treated rats was investigated. Male Sprague-Dawley rats were randomly divided into three groups: a saline group, a heroin and saline group, and a heroin and sodium hydrosulfide group. According to the principle of increasing heroin dosage daily, heroin withdrawal was precipitated on day 9 with an injection of naloxone (5 mg/kg, i.p.), and withdrawal symptoms were scored. The levels of cystathionine-${eta}$-synthase, $H_2S$, reduced glutathione and malondialdehyde, as well as the levels of cleaved caspase-3, Bax, and Bcl-2 proteins and the activities of superoxide dismutase, catalase, and glutathione peroxidase were assayed in the hippocampus. The results showed that exogenous $H_2S$ alleviated heroin withdrawal symptoms. Moreover, exogenous $H_2S$ not only increased cellular $H_2S$ and the cystathionine-${eta}$-synthase protein level activity but also significantly improved heroin-induced oxidative stress. Protein expression of cleaved caspase-3 and Bax decreased, whereas Bcl-2 protein levels in hippocampus increased with exogenous $H_2S$. Exogenous $H_2S$ alleviated heroin-induced rat hippocampal damage through antioxidant and antiapoptosis effects.